Combination Therapies With Insulin in Type 2 Diabetes

Yki‐Järvinen, Hannele

doi:10.2337/diacare.24.4.758

Cited by 266 publications

(174 citation statements)

References 61 publications

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“…There are few studies of an oral agent added to insulin therapy in patients with comparable phenotype, thus direct comparisons are problematic [7]. In studies of patients most closely resembling the participants in the present study, it becomes apparent that somewhat greater efficacy may be achieved at the expense of undesirable side effects.…”

Section: Discussionmentioning

confidence: 81%

“…In a 16-week study, metformin titrated to 2,550 mg/day decreased HbA 1c by 0.6%, but with a twofold increase in severe hypoglycaemia and a more than fourfold increase in gastrointestinal adverse events [9]. When data from seven disparate studies of a sulfonylurea added to insulin were pooled, it appeared that sulfonylurea reduced HbA 1c by 0.3% relative to placebo [7], similar to vildagliptin in the overall cohort. However, direct comparisons would be necessary to achieve a more complete understanding of the relative effectiveness and tolerability of different oral agents in combination with insulin.…”

Section: Discussionmentioning

confidence: 99%

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Addition of vildagliptin to insulin improves glycaemic control in type 2 diabetes

et al. 2007

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Aims/hypothesis Type 2 diabetes is difficult to manage in patients with a long history of disease requiring insulin therapy. Moreover, addition of most currently available oral antidiabetic agents increases the risk of hypoglycaemia. Vildagliptin is a dipeptidyl peptidase-IV inhibitor, which improves glycaemic control by increasing pancreatic beta cell responsiveness to glucose and suppressing inappropriate glucagon secretion. This study assessed the efficacy and tolerability of vildagliptin added to insulin therapy in patients with type 2 diabetes. Materials and methods This was a multicentre, 24-week, double-blind, randomised, placebo-controlled, parallelgroup study in patients with type 2 diabetes that was inadequately controlled (HbA 1c =7.5-11%) by insulin. Patients received vildagliptin (n=144; 50 mg twice daily) or placebo (n=152) while continuing insulin therapy.Results Baseline HbA 1c averaged 8.4 ± 0.1% in both groups. The adjusted mean change from baseline to endpoint (AMΔ) in HbA 1c was −0.5±0.1% and −0.2± 0.1% in patients receiving vildagliptin or placebo, respectively, with a significant between-treatment difference (p=0.01). In patients aged ≥65 years, the AMΔ HbA 1c was −0.7±0.1% in the vildagliptin group vs −0.1±0.1% in the placebo group (p<0.001). The incidence of adverse events was similar in the vildagliptin (81.3%) and placebo (82.9%) groups. However, hypoglycaemic events were less common (p<0.001) and less severe (p<0.05) in patients receiving vildagliptin than in those receiving placebo. Conclusions/interpretation Vildagliptin decreases HbA 1c in patients whose type 2 diabetes is poorly controlled with high doses of insulin. Addition of vildagliptin to insulin therapy is also associated with reduced confirmed and severe hypoglycaemia. ClinicalTrials.gov ID no.: NCT 00099931.

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Section: Discussionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Addition of vildagliptin to insulin improves glycaemic control in type 2 diabetes

et al. 2007

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“…The cost is surprisingly similar as well, owing to the differences in total insulin dose that will be needed to achieve control (i.e., continuing oral agents will result in less insulin being needed) (table 3). 62,63 Continuation of metformin makes intuitive sense, as its mechanism compliments that of insulin and tends to lessen any weight gain that might occur. On the contrary, an SU works in relatively the same manner as insulin and thus is often discontinued.…”

Section: Triple Oral Therapy or Insulin Initiation?mentioning

confidence: 99%

Current Therapeutic Options in Type 2 Diabetes Mellitus: A Practical Approach

Sheehan¹

2003

Clinical Medicine & Research

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The incidence of type 2 diabetes mellitus (DM) in the United States continues to grow rapidly, paralleling the overweight and obesity epidemic. For many years the only therapeutic options for type 2 DM were sulfonylureas and insulin. However, over the last 9 years there has been an explosion of new and exciting agents approved for the treatment of type 2 DM. Some of the treatments target insulin deficiency and others insulin resistance, the hallmarks of the disease. Other drugs delay the intestinal absorption of carbohydrate. Recently several combination agents have been released. With these new drugs has come an overwhelming mountain of information, making it difficult for the busy clinician to know how best to manage the ever-increasing portion of patients with type 2 DM.New questions have arisen: Which agent to start as first line? How much of this drug to use before adding something else? How long for this drug to reach full effect? Which agent to add second? Should a patient uncontrolled on dual therapy begin insulin or start a third oral agent? If insulin therapy is started, what should become of the patient's oral agents? How best to explain the patient's weight gain on therapy? These are not easy questions and no review can fully detail all the therapeutic combinations possible. Instead, the practical approach of reviewing the agents in terms of their mechanism of action and critically comparing their dosing, effect and cost, is undertaken herein. Also addressed is the possible niche some newer classes of agents and combination drugs may or may not hold in the management of type 2 DM. The decision of using insulin versus a third oral agent will be looked at from the standpoint of where the patient is on dual therapy in relation to the hemoglobin A 1c goal. In this way it is hoped that some clarity will be brought to the dizzying array of information that both the physician and patient have to deal with in regard to the management of this prevalent and serious disease.

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“…1,2 However, treatment with oral antidiabetic agents (OADs) is associated with undesirable side-effects such as GI intolerance, weight gain, peripheral oedema, osteoporotic fracture or hypoglycaemia. 3,4 Moreover, the use of OADs either alone or in combination is limited by their inability to sustain glycaemic control over time. 5 When the combination of OADs fails to achieve glycaemic targets, the conventional approach is to add insulin.…”

Section: T Ype 2 Diabetes Mellitus (T2dm)mentioning

confidence: 99%